Skin inflammation in Sharpin-deficient mice is primarily due to TNFR1-dependent apoptosis, but necroptosis appears to play a bigger role in inflammation of internal organs.
A link between chronic stress and organ dysfunction is explained by the gateway reflex, in which brain micro-inflammation at specific vessels establishes a new neural pathway to induce fatal organ failure particularly in gastrointestine and heart.
During aging, the pancreatic endocrine islets undergo chronic inflammation, which is associated with a reduced capacity for self-renewal of the insulin-producing beta-cells in zebrafish.
Reduced energy expenditure in obesity may result from reduced sensitivity to sympathetic activation due to inflammation-generated signals in adipose tissue.
The adaptor proteins FADD and TRADD play an important role in the Sharpin-dependent anti-apoptosis signaling pathway in keratinocytes and regulate skin homeostasis.
Editors' Summary: This Replication Study has reproduced some parts of the original paper but it also contains results that are not consistent with other parts of the original paper.
Impaired autophagy influences intestinal inflammation and hypersensitivity responses by orchestrating mucosal T cell populations, suggesting new translational perspectives for the treatment of these conditions.
